Re: Bacteria + high-fat diet/genetic susceptibility promote atherosclerosis

[Guest guest]

Roman-

I'm not inclined to pay much attention to this study for a couple reasons,

though to be fair I didn't pay $15 to read the full text.

First, and perhaps most importantly, mice are not people. Animal tests

_can_ be useful, but they're a minefield of species-specific results. In

fact, there's a very good argument against using them at all at

http://www.sumeria.net/health/prism.html -- specifically because of the

toll on human health that results from relying on them. For example, if

you know what you're doing, you can pick the species that will give you the

result you want in " testing " a new drug for safety. So the question to ask

when looking at these dietary studies based on animal results is, how well

do those animals map to people? Specifically, is their natural diet

anything like the natural diet of humans? In the case of mice, the answer

is pretty clear: I don't think so! Remember the study that helped kick off

the cholesterol theory -- it involved feeding rabbits, which are

herbivores, tons of oxidized cholesterol! Oxidized cholesterol probably

isn't good for any animal, but drawing conclusions about what omnivores

should eat from the results of feeding herbivores a substance found only in

animal foods is absurd.

Second, what exactly were these mice fed? Perhaps the full text of the

study would tell us, perhaps not, but " high fat " can mean all kinds of

things. Perhaps the mice were fed margarine. Perhaps they were fed

damaged animal fats. Perhaps they were stuffed so full of fat that no

animal could've thrived, or even survived. Regardless, I'd guess it's

highly unlikely that the mice were fed species-appropriate fat in

species-appropriate quantities. I'm not sure what the diet of lab mice in

the wild is, but it probably doesn't at all resemble their lab feed.

>The original study report can be found here:

>abstract -

>http://circ.ahajournals.org/cgi/content/abstract/105/7/861

>-- free

>full text -

>http://circ.ahajournals.org/cgi/content/full/105/7/861

>-- not free

-

[Guest guest]

>This doesn't sound good.

>

>http://www.mercola.com/2002/mar/20/gum_disease.htm

>

>I hope somebody can analyze the study and find a

>serious flaw in it.

Weeelll...how many people get injected with plaque bacteria? How does

that compare with the number of bacteria that would work themselves

into the bloodstream from the mouth? There has been some correlation

between gum disease and c-v disease, but post hoc non propter

hoc...they're both caused by faulty diet.

[Guest guest]

Heart disease and gum disease are both linked with major dietary

flaws it would seem obvious tha both tissues would be weakend

immunologically and suceptible to infection. As usual the " science "

hear has a difficulty with the concept of cause and effect and also

as usual has placed the effect and the horse ahead of the cause and

the cart.

DMM

> >This doesn't sound good.

> >

> >http://www.mercola.com/2002/mar/20/gum_disease.htm

> >

> >I hope somebody can analyze the study and find a

> >serious flaw in it.

>

> Weeelll...how many people get injected with plaque bacteria? How

does

> that compare with the number of bacteria that would work themselves

> into the bloodstream from the mouth? There has been some

correlation

> between gum disease and c-v disease, but post hoc non propter

> hoc...they're both caused by faulty diet.

[Guest guest]

The experiment does not indict a high-fat diet. Differant animals

respond to dietary fat and cholesterol differant. Omnivores and

carnivores don't - you can feed them fat and cholesterol until the

cows come home (and then feed them the cows), and their cholesterol

will hardly budge. That is also how it is for humans - adopting the

american heart association step 1 diet will only lower cholesterol by

about 5% (BMJ 1997;314:112-117).

However, vegetarian animals will see massive increases in cholesterol

as the cholesterol piles up in the liver, spleen(New Zealand Medical

Journal, 1988, 101, 795.) as well as the arteries. This is not true

atherosclerosis, which only happens where blood flow becomes

turbulant, which are the places where the arteries form branches or

sharp bends(Progress in Cardiovascular Disease 33 (2), sep/oct 1990,

119-36).

Researchers know this, and the study is actually a sign of that

knowledge. It is becoming increasingly believed that heart disease is

the result of chronic inflammation of the arteries. A bacterial

infection is one of the more novel proposed sources of inflammation,

and that is what the researchers were interested in studying.

However, 50 years of feeding egg yolks to rabbits dies hard, and many

researchers still insist on accomanying the study of inflammation

with a high-fat diet given to a vegetarian animal.

Another proposed sources of the inflammation is through direct injury

to the artery. If you dig through medline, you can find many similar

studies in which the arteries are damaged with an inflatable balloon,

and then the inevitable cholesterol feeding.

None of these studies will tell us very much, because the cholesterol

feeding does not properly reproduce atherosclerosis. The best animal

models involve surgically altering the shape of the animals arteries

to induce turbulant blood flow. (Circ Res. 1997;81:328-337), this

correctly reproduces atherosclerosis *and* explains the very specific

locations in the arteries where it is found.

The big picture is this: most researchers are now studying the role

of cholesterol + something else (where something else may be

inflammation, damage to the arteries, endothelial dysfunction etc...)

instead of just cholesterol. Baby steps. One day they may jetison

cholesterol entirely and we'll be able to treat and prevent heart

disease!